A research team led by Dr. Alon Chen of the Weizmann Institute’s Neurobiology Department has discovered that changes in the activity of a single gene in the brain not only cause mice to exhibit anxious behavior, but also lead to metabolic changes that cause the mice to develop symptoms associated with type 2 diabetes. These findings were published online this week in the Proceedings of the National Academy of Sciences (PNAS).
The researchers developed a new, finely-tuned method for influencing the activity of a single gene in one area in the brain, using it to increase the amounts of Ucn3, protein produced in certain brain cells especially in times of stress. This protein is known to play a role in regulating the body’s stress response. The researches found that heightened levels of Ucn3 produced two different effects: The anxiety-related behavior of the mice increased, and their bodies underwent metabolic changes as well. With excess Ucn3, their bodies burned more sugar and fewer fatty acids, and their metabolic rate sped up. These mice began to show signs of the first stages of type 2 diabetes: A drop in muscle sensitivity to insulin delayed sugar uptake by the cells, resulting in raised sugar levels in the blood. Their pancreases then produced extra insulin to make up for the perceived ‘deficit.’
According to Dr. Chen this mechanism may in the future point the way toward the treatment or prevention of a number of stress-related diseases.